1

RATIONALE OF ENDODONTIC
TREATMENT
 Contents of these presentation 2

 INTRODUCTION
 THEORIES OF SPREAD OF INFECTION
 CULPRIT OF ENDODONTIC PATHOLOGY
 PORTALS FOR ENTRY OF MICROORGANISMS
 INFLAMMATION
 TISSUE CHANGES FOLLOWING INFLAMMATION
 INFLAMMATORY CELLS
 INFLAMMATORY RESPONSE TO PERIAPICAL LESION
 ANTIBODIES (SPECIFIC MEDIATORS OF IMMUNE REACTIONS)
 ROLE OF IMMUNITY IN ENDODONTICS
 ENDODONTIC IMPLICATIONS (PATHOGENESIS OF APICAL PERIODONTITIS AS
EXPLAINED BY FISH)
 KRONFELD’S MOUNTAIN PASS THEORY
 RATIONALE OF ENDODONTIC THERAPY
INTRODUCTION 3

 Endodontic pathology is caused by

 Physical , chemical or bacterial injury
 These injury results in reversible or irreversible changes in the
pulp & periradicular tissues.
 Changes depends on the
o Intensity , duration , pathogenicity of the stimulus and
o host defense mechanism
 Changes mediated by a series of inflammatory & immunological
reactions
 All these reaction take place to eliminate the irritant and repair
any damage
 However, certain conditions are beyond the reparative ability of
the body and need to be treated endodontically to aid the
survival of tooth
 Rationale of endodontic therapy is complete debridement of
root canal system followed by three-dimensional obturation
THEORIES OF SPREAD OF 4

INFECTION
 Focal Infection
Definition: It is localized or general infection caused by the
dissemination of microorganisms or toxic products from a focus
of infection.
 Focus of Infection
Definition: This refers to a circumscribed area of tissue,
which is infected with exogenous pathogenic microorganisms
and is usually located near a mucous or cutaneous surface.
 Theory Related to Focal Infection
 William Hunter first suggested that oral microorganisms and their
products involved in number of systemic diseases, are not always
of infectious origin.
 In year 1940, Reimann and Havens criticized the theory of focal
infection with their recent findings
Cont of theories 5

Mechanism of Focal Infection

There are generally two most accepted mechanisms considered

responsible for initiation of focal infection:
1. Metastasis of microorganisms from infected focus by either
hematogenous or lymphogenous spread.
2. Carrying of toxins or toxic byproducts through bloodstream
and lymphatic channel to site where they may initiate a
hypersensitive reaction in tissues.

For example: In scarlet fever, erythrogenic toxin liberated by

infected streptococci is responsible for cutaneous features of this
disease.
Cont of theories 6

Oral Foci of Infection

Possible sources of infection in oral cavity which later on may set up
distant metastases are:
1. Infected periapical lesions such as:
i. Periapical granuloma
ii. Periapical abscess
iii. Periapical cyst
2. Teeth with infected root canals.
3. Periodontal diseases with special reference to tooth extraction.
CULPRIT OF ENDODONTIC 7

PATHOLOGY

 Root canal infections are multibacterial in nature.

 In 1965, Kakehashi describe the Importance of
microorganisms for the development of pulpal and
periapical pathologies
PORTALS FOR ENTRY OF 8

MICROORGANISMS
 Microorganisms may gain entry into pulp through
o Most common route for entering of microorganisms to dental
pulp is dental caries
 Microorganisms can pass into the dentinal tubules and subsequently
to the pulp resulting in its necrosis
 Through the periodontal ligament or the gingival sulcus,
microorganisms can enter into the pulp via accessory and lateral
canals which connect pulp and the periodontium
o Entry into pulp cavity via mechanical or traumatic injury,
through gingival sulcus and via bloodstream
o Anachoresis
 Anachoresis refers to the attraction of blood borne bacteria in the
areas of inflammation
 Microorganisms are transported in the blood to an area of
inflammation where they establish an infection.
o Through defective restorations, faulty restoration with marginal
leakage can result in contamination of the pulp by bacteria.
 Cont of portal of entry 9

Fig. : Deep carious lesion

Fig. : Radiograph resulting in pulp necrosis and
showing poorly periapical lesion
obturated canals
 INFLAMMATION 10

 Inflammation is defined as the local response of living

mammalian tissue to injury due to any agent.
 Agents that cause inflammation
 Physical
 Cold, heat, echanical trauma or radiation
 Chemical
• organic and inorganic poisons
 Infective
• bacteria, viruses and their toxins
 Immunological
• antigen-antibody cell mediated reactions
 inflammation is distinct from infection. Inflammation is the
protective response by the body,
 while infection is invasion into the body by harmful microbes and
their resultant ill effects by toxins
Cont of inflammation 11

Signs of Inflammation
 The roman writer celsus in 1st century AD gave four
cardinal signs of inflammation:
1. Rubor i.e. redness
2. Tumor i.e. swelling
3. Color i.e. heat
4. Dolor i.e. pain
 Virchow later added the fifth sign of inflammation
function lasea,
i.e. loss of function
Cont of inflammation 12

Inflammation is of Two Types

1. Acute inflammation
o dominated by PMNLs (Polymorphonuclear lymphocytes)
and few macrophages
2. Chronic inflammation
o dominated by lymphocytes, macrophages and plasma cells.
 The balance between the host defense and microbial
factor determines the formation of lesion
 TISSUE CHANGES FOLLOWING
13
INFLAMMATION
1. Degenerative changes
 The pulp can be:
 Fibrous, Resorptive and Calcific

 Continuous degeneration of the tissue results in necrosis.

 Suppuration
 is another form of degeneration which is due to injury to polymorphonuclear cells.

 It causes release of proteolytic enzymes with resulting liquefaction of dead

tissues thus leading to formation of pus or suppuration.

 Three requisites which are necessary for suppuration

 Tissue necrosis
 Polymorphonuclear leukocytes
 Digestion of the necrotic material by proteolytic enzymes released by
injured polymorphonuclear cells
Clinical significance:
An abscess can result even in absence of
microorganisms because of chemical or physical irritation. It results in
formation of sterile abscess
Cont of tissue changes 14

2. Proliferative changes
 The irritant may be strong enough to produce
degeneration or destruction, whereas at the periphery,
the irritant may be mild enough to stimulate proliferation.
 The principal cells are
 Fibroblasts, which lay down cellular fibrous tissues.
 In some cases collagen fibers may be substituted by a dense
acellular tissue.

 In either case it results in formation of fibrous

tissue.
INFLAMMATORY CELLS 15

1. Neutrophils
2. Eosinophils
3. Lymphocytes
4. Osteoclasts
5. Ephithelial
cells
Inflammatory Response to 16
Periapical Lesion
Nonspecific Mediators of Periradicular Lesions

can be classified into following types:

1. Cell derived mediators:
– Neuropeptides
– Eicosanoids/arachidonic
acid derivatives
– Cytokines
– Lysosomal enzymes
– Platelet activating factor
– Vasoactive amines
– Prostaglandins
2. Plasma derived mediators
– The fibrinolytic system
– The complement system
– The kinin system
3. Extracellular matrix derived
mediators
– Effector molecules
Antibodies (Specific Mediators of 17
Immune Reactions)
 These are produced by plasma cells and are of two types
1. Polyclonal antibodies
 are nonspecific like IgE mediated reactions which interact
with antigen resulting in release of certain chemical
mediators like histamine or serotonin
2. Monoclonal antibodies
 like IgG and IgM, interact with the bacteria and its by-
products to form antigen-antibody complexes that bind to
the platelets resulting in release vasoactive amines thus
increasing the vascular permeability and chemotaxis of
PMNs.
 The monoclonal antibodies exhibit antimicrobial effect.
 In acute abscess, the complex enters the systemic
circulation. The concentration of these complexes return
to normal levels after endodontic treatment.
 In chronic lesions, the Ag-Ab complexes are confined
within the lesion and do not enter into the systemic
circulation
Cont.… 18

 The response of periapical/host tissue is

controlled by:
 Cells

 Molecular mediators (Nonspecific

mediators of inflammation), and
 Antibodies(Specific mediators of
inflammation)
 Role of Immunity in 19
Endodontics

 Immunity is of two types:

1. Innate immunity
2. Acquired/adaptive immunity

1. Innate immunity
 It is responsible for the initial nonspecific reactions.
 Cells providing innate immunity are neutrophils, monocytes, eosinophils,
basophils, NK cells, dendritic cells, and odontoblasts.
 20

2. Acquired/Adaptive immunity
 It involves release of specific receptor molecules by
lymphocytes which recognize and bind to foreign
antigens.

 Adaptive immunity is provided by:

 T-Lymphocytes that release T-cell antigen receptors
 B-Lymphocytes that release B-cell antigen receptors or immunoglobulins.
 21
ENDODONTIC IMPLICATIONS (PATHOGENESIS
OF APICAL PERIODONTITIS AS EXPLAINED BY
FISH)

 FISH described the reaction of the periradicular tissues to bacterial

products, noxious products of tissue necrosis, and antigenic agents
from the root canal

 FISH in 1939 theorized that the zones of infection are not an infection
by themselves but the reaction of the body to infection.
Thus he concluded that the removal of this nidus of infection will
result in resolution of infection.
 22

 Four well defined zones of reaction

were found during the experiment
a. Zone of infection or necrosis (PMNLs)
b. Zone of contamination (Round cell
infiltrate – lymphocytes)
c. Zone of irritation (Histiocytes and
osteoclasts)
d. Zone of stimulation (Fibroblasts,
capillary buds and Osteoblasts).

Fig: FISH zones

 23

Zone of Infection
 Infection was confined to the center of the lesion.
 This zone is characterized by polymorphonuclear leukocytes and
microorganisms along with the necrotic cells and detructive
components released from phagocytes.
Zone of Contamination
 Area of cellular destruction.
 This zone was not invaded by bacteria, but the destruction was
from toxins discharged from the microorganisms in the central
zone.
 This zone is characterized by round cell infiltration, osteocyte
necrosis and empty lacunae.
 Lymphocytes were prevalent everywhere.
 24

Zone of Irritation
 FISH observed evidence of irritation further away from the central lesion as
the toxins became more diluted.
 This is characterized by macrophages, histocytes and osteoclasts.
 The degradation of collagen framework by phagocytic cells and
macrophages was observed while osteoclasts attack the bone tissue.
 The histologic picture is much like preparatory to repair.
Zone of Stimulation
 FISH noted that, at the periphery, the toxin was mild enough to act as
stimulant.
 This zone is characterized by fibroblasts and osteoblasts.
 In response to this stimulatory irritant, fibroblasts result in secretion of
collagen fibers, which acted both as wall of defense around the zone of
irritation and as a scaffolding on which the osteoblasts synthesize new
bone.
 25

 The knowledge gained in FISH study can be applied for better

understanding of reaction of periradicular tissues to a nonvital tooth.
 The metabolic byproducts of these microorganisms or the toxic products of
tissue necrosis may also get diffused to the periradicular tissues.
 As the microorganisms enter in the periradicular area, they are destroyed
by the polymorphonuclear leukocytes.
But if microorganisms are highly virulent, they overpower the
defensive mechanism and result in development of periradicular lesion.
 The toxic byproducts of the microorganisms and the necrotic pulp in the
root canal are irritating and destructive to the periradicular tissues. These
irritants along with proteolytic enzymes (released by the dead
polymorphonuclear leukocytes) result in the formation of
 chronic abscess
 Granuloma
 Sclerotic bone and then
 Cyst
Kronfeld’s Mountain 26
Pass Theory
 Kronfeld explained that the granuloma does not
provide a favorable environment for the survival
of the bacteria

Zone A:
He compared the bacteria in the infected root canal
with the invaders entrenched behind high and inaccessible
“mountains”, the foramina serving as mountain passes.

Zone B:
The exudative and granulomatous (proliferative)
tissue
of the granuloma represents a mobilized army defending
the
plains (periapex) from the invaders (bacteria). When a few
invaders enter the plain through the mountain pass, they
are
destroyed by the defenders (leukocytes). A mass attack of
invaders results in a major battle, analogous to acute
inflammation.
 27

Zone C:
Only complete elimination of the invaders from their
mountainous entrenchment will eliminate the need for a defense
forces in the “plains”. Once this is accomplished, the defending
army of leukocytes withdraws, the local destruction created by
the battle is repaired (granulation tissue) and the environment
returns to its normal pattern

 This explains the rationale for the non-surgical

endodontic treatment for teeth with periapical
infection. The complete elimination of
pathogenic irritants from the canal followed by
the three-dimensional fluid impervious
obturation will result in complete healing of
periapical area
Rationale of Endodontic 28

Therapy
 The rationale of RCT relies on the fact that the nonvital pulp,
being avascular, has no defense mechanisms
 The damaged tissue within the root canal undergoes
autolysis and the resulting breakdown products will diffuse
into the surrounding tissues and cause periapical irritation
associated with the portals of exit even in the absence of
bacterial contamination.
 It is essential therefore, that endodontic therapy must seal
the root canal system three-dimensionally so as to prevent
tissue fluids from percolating in the root canal and toxic
byproducts from both necrotic tissue and microorganisms
regressing into the periradicular tissues.
 29

Endodontic therapy includes:

 Non-surgical endodontic treatment

 Surgical endodontic treatment

 30

Non-surgical endodontic treatment includes three phase

1. Access preparation
2. Shaping and cleaning
3. Obturation
Surgical Endodontic Treatment
 The rationale of surgical endodontics is to remove the diseased
tissue present in the canal and around the apex, and retrofil the
root canal space with biologically inert material so as to achieve a
fluid tight seal.